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DTSTART:19960101T000000 END:STANDARD BEGIN:STANDARD TZNAME:GMT TZOFFSETFROM:+0100 TZOFFSETTO:+0000 DTSTART:19961027T020000 RRULE:FREQ=YEARLY;BYMONTH=10;BYDAY=-1SU END:STANDARD END:VTIMEZONE BEGIN:VEVENT DTSTAMP:20260511T050913Z DTSTART;VALUE=DATE-TIME:20210512T130000 DTEND;VALUE=DATE-TIME:20210512T140000 SUMMARY:BMS Divisional Webinar: The Life and Times of a Macrophage: Only the Good Die Young? Dr Stephen Jenkins\, Centre for Inflammation Researc h\, Edinburgh Medical School TZID:Europe/London UID:20210512-8a17841b756ec68b01756eeb537f0112@warwick.ac.uk CREATED:20210504T145843Z DESCRIPTION:Abstract: Certain populations of tissue-resident macrophages are maintained by self-renewal and longevity while others are continuall y replenished from circulating monocytes\, yet the basis for these tissu e-specific differences and the downstream effect on macrophage function is unclear. Furthermore\, inflammation generally leads to recruitment of abundant monocyte-derived macrophages\, but what regulates the fate of these cells and the extent to which they can assume the identity and fun ction of resident macrophages also remains unclear. To address these que stions\, we have studied the factors governing the behaviour of peritone al macrophages. We have found that under non-inflamed conditions\, reple nishment of peritoneal macrophages from the bone marrow occurs in a sexu ally dimorphic manner and that this leads to sex-differences in macropha ge phenotype and ability to protect against peritonitis. These data esta blish that the rate-of-replenishment from the bone marrow plays a key ro le in the function of tissue-resident macrophages and highlights the imp ortance of considering both sex and age in susceptibility to inflammator y and infectious diseases. Following inflammation\, we found that recrui ted monocyte-derived inflammatory macrophages persist long-term but in a n immature transitory state of differentiation that is characterised by defective responsiveness to secondary immune challenge. Critically\, rat her than being pre-programmed this immature state was a direct consequen ce of the presence of enduring established resident macrophages. Hence\, competitive pressure between incoming monocytes and established tissue resident macrophages may an underlying driving force for the evolution o f tissue-resident macrophage autonomy. These data have major implication s for understanding the long-term effects of inflammation on tissue heal th and responsiveness to future disease. Biography: Steve Jenkins is a L ecturer at the University of Edinburgh’s Centre for Inflammation Researc h. He obtained his PhD in Parasite Immunology at the University of York before undertaking post-doctoral research with Profs Andrew MacDonald an d Judith Allen at the University of Edinburgh on the regulation of adapt ive and innate immune responses during helminth infection. During this t ime he discovered of an alternative process of inflammation whereby macr ophages increase in number independently of monocyte recruitment through rapid proliferation of tissue resident cells (Science\, 2011\, PMC31284 95\; J Ex Med\, 2013\, PMC3804948)\, which helped stem a major re-assess ment of the ontogeny of macrophages during homeostasis and disease. He s ubsequently moved the University of Edinburgh’s Centre for Inflammation Research to establish his own research group focusing on how macrophage survival\, proliferation and function is regulated during inflammatory d isease\, and received tenure in 2016. His recent work has included defin ing the effect of cell origin\, time-in-tissues\, inflammation exposure\ , and biological sex on the function and proliferative capacity of tissu e macrophages\, and how this effects resistance to bacterial infection. MS Teams link available here: /fac/sci/med/staffint ranet/divisions/bms/virtual_community LOCATION:via Teams CATEGORIES:BiomedicalSciences,DivisionalSeminars LAST-MODIFIED:20210504T145843Z ORGANIZER;CN=Jas Bains: END:VEVENT END:VCALENDAR